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Transition from Acute to Chronic Pain

Last updated 1 Jun 2026 · Pain & analgesia

📋 Key Information Summary

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  • Approximately 10–50% of patients undergoing surgery or experiencing significant acute injury develop chronic post-surgical pain (CPSP) or chronic pain, representing a major public health burden in Australia.
  • Severe acute pain intensity is the strongest modifiable predictor of chronic pain transition — inadequate early analgesia increases risk.
  • Neuropathic mechanisms (peripheral and central sensitisation) underpin the transition; screening for neuropathic features early (e.g., DN4 ≥ 4) guides targeted therapy.
  • Catastrophising and psychological vulnerability (anxiety, depression, fear avoidance) are independent risk factors — address with early psychological input.
  • Central sensitisation involves amplified spinal cord and supraspinal nociceptive processing; manifests as hyperalgesia, allodynia, and pain beyond the expected tissue territory.
  • Preventive strategies should commence peri-operatively: multimodal analgesia, gabapentinoids or ketamine in high-risk patients, and early psychological screening.
  • Gabapentin (Neurontin®) and pregabalin (Lyrica®) have evidence for CPSP prevention when started peri-operatively; PBS-listed for neuropathic pain.
  • Intra-operative IV ketamine (sub-anaesthetic doses 0.25–0.5 mg/kg) reduces CPSP incidence in high-risk surgical patients.
  • Regional anaesthesia (e.g., epidural, peripheral nerve blocks) when feasible reduces acute pain severity and may lower CPSP risk.
  • Screen all post-surgical patients at 3–6 months with the Brief Pain Inventory (BPI) or DN4 to identify those transitioning to chronic pain for early intervention.
  • Aboriginal and Torres Strait Islander Australians experience higher rates of chronic pain with delayed access to multidisciplinary services — culturally safe, early intervention is essential.
  • Avoid prolonged opioid use beyond the acute phase without clear reassessment — opioid continuation beyond 6 weeks post-surgery is a risk factor for chronicity.

Introduction & Australian Epidemiology

Chronic pain — defined by the International Association for the Study of Pain (IASP) as pain persisting or recurring for more than three months — is one of the leading causes of disability in Australia. The Australian Institute of Health and Welfare (AIHW) estimates that chronic pain affects approximately 3.4 million Australians, costing the economy over 9 billion annually when productivity losses are included.

The transition from acute to chronic pain is not merely persistence of nociceptive input. Rather, it reflects a complex neurobiological and psychosocial process in which peripheral and central nervous system plasticity, psychological state, and genetic susceptibility converge. After surgery, chronic post-surgical pain (CPSP) develops in 10–50% of patients depending on the procedure (highest after thoracotomy, amputation, mastectomy, and inguinal hernia repair). After musculoskeletal injury, whiplash, and lower back trauma, rates of chronicity are similarly high.

This article reviews the risk factors for transition, the role of neuropathic mechanisms and central sensitisation, and evidence-based prevention strategies applicable to Australian primary care and hospital settings.

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Key concept: The transition to chronic pain is a disease process in its own right — not simply "unresolved acute pain." Early identification and intervention are critical to improving outcomes.

Risk Factors

Risk factors for the transition from acute to chronic pain are multifactorial and can be categorised into patient-related, pain-related, surgery/procedure-related, and psychosocial domains. Identifying high-risk patients early allows targeted preventive interventions.

Low Risk
Modifiable factors absent
Mild–moderate acute pain (NRS < 5), no prior chronic pain, no psychological comorbidity, minor procedure, no neuropathic features.
Setting: Standard peri-operative pathway
Moderate Risk
1–2 risk factors present
Moderate acute pain (NRS 5–7), mild catastrophising, prior chronic pain elsewhere, moderate surgical insult (e.g., abdominal surgery), early neuropathic features.
Setting: Enhanced monitoring, consider gabapentinoid
High Risk
≥ 3 risk factors present
Severe acute pain (NRS ≥ 7), high catastrophising (PCS ≥ 30), pre-existing chronic pain, major surgery (thoracotomy, amputation, mastectomy), significant neuropathic component, anxiety/depression, opioid use > 48 h.
Setting: Multimodal prevention protocol, psychology referral, pain medicine review

Patient-Related Risk Factors

Factor Evidence Australian Relevance
Female sex Consistent association with CPSP in meta-analyses (OR 1.3–1.6) Higher chronic pain prevalence reported in Australian women (AIHW 2020)
Younger age Paradoxical association — younger adults have higher CPSP rates than elderly May reflect greater surgical aggressiveness and nerve preservation challenges
Pre-existing chronic pain OR 2.0–3.5 for developing CPSP Central sensitisation already established; manage existing pain optimally pre-operatively
Genetic susceptibility COMT Val158Met, SCN9A, GCH1 polymorphisms Not yet routine in Australian practice; pharmacogenomics emerging
Obesity (BMI ≥ 30) OR 1.4 for persistent pain after surgery 31% of Australian adults are obese (ABS 2022); contributes to inflammation

Pain-Related Risk Factors

  • Severe acute pain (NRS ≥ 7/10) — the single strongest modifiable predictor of chronicity. Undertreated acute pain drives peripheral and central sensitisation.
  • Neuropathic pain features (burning, shooting, tingling, allodynia) — presence of neuropathic pain in the acute phase doubles chronic pain risk.
  • Widespread pain / secondary hyperalgesia — pain spreading beyond the surgical/injury site suggests central sensitisation is already occurring.
  • Opioid use beyond 48 hours — prolonged opioid exposure paradoxically sensitises the nervous system (opioid-induced hyperalgesia).

Psychosocial Risk Factors

  • Pain catastrophising (Pain Catastrophising Scale [PCS] ≥ 30) — rumination, magnification, helplessness. OR 2.5–3.0 for chronic pain development.
  • Depression and anxiety — bidirectional relationship; pre-existing mood disorder amplifies pain processing. Screen with PHQ-9, GAD-7.
  • Fear avoidance beliefs — expectation that activity will cause further damage leads to disuse, deconditioning, and pain chronification.
  • Poor social support — isolation and lack of practical support during recovery independently predict poor outcomes.
  • Workplace factors — litigation, workers' compensation claims, job dissatisfaction increase chronic pain risk (particularly relevant for workplace injuries in Australia).

Surgery/Procedure-Related Risk Factors

Procedure CPSP Incidence Key Risk Factor
Amputation 50–85% (phantom limb pain) Nerve transection, pre-amputation pain
Thoracotomy 30–50% Intercostal nerve injury, rib spreading
Breast surgery (mastectomy) 20–50% Intercostobrachial nerve injury, axillary dissection
Inguinal hernia repair 10–30% Ilioinguinal/genitofemoral nerve injury, mesh-related
Total knee replacement 10–20% Pre-existing central sensitisation, inadequate rehabilitation
Caesarean section 5–18% Acute pain severity, wound complications, psychological distress
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Critical action: All patients scheduled for high-risk surgery (thoracotomy, amputation, mastectomy, hernia repair) should undergo pre-operative psychological screening (PCS, PHQ-9, GAD-7) and receive a preventive multimodal analgesia protocol.

Neuropathic Component

Neuropathic pain — defined as pain caused by a lesion or disease of the somatosensory nervous system — is a critical driver of the acute-to-chronic pain transition. In the peri-operative setting, nerve injury (surgical transection, compression, traction, thermal injury) initiates a cascade of peripheral and central changes that, if unchecked, establish chronic neuropathic pain.

Peripheral Mechanisms

  • Peripheral sensitisation: Tissue damage releases inflammatory mediators (bradykinin, prostaglandins, substance P, NGF) that lower the activation threshold of nociceptors (Aδ and C fibres). This accounts for primary hyperalgesia at the wound site.
  • Neuroma formation: After nerve transection, regenerating axons form disorganised neuromas with ectopic firing — spontaneous pain and mechanical allodynia. This is the hallmark of post-surgical neuropathic pain (e.g., intercostobrachial neuralgia after mastectomy).
  • Sodium channel upregulation: Damaged nerves overexpress Nav1.3, Nav1.7, and Nav1.8 sodium channels, generating spontaneous ectopic discharges. This explains the efficacy of sodium channel blockers (lignocaine) and certain anticonvulsants.
  • Sympathetic coupling: Noradrenaline from sympathetic efferents can sensise damaged nociceptors, contributing to sympathetically maintained pain and complex regional pain syndrome (CRPS).

Screening for Neuropathic Pain

Early identification of neuropathic features in the acute setting is essential. The following validated tools are available in Australian practice:

Essential DN4 Questionnaire (Douleur Neuropathique 4) 7 items (interview) + 2 clinical tests (brush allodynia, pinprick hypoesthesia). Score ≥ 4/10 = neuropathic pain likely. Sensitivity 83%, specificity 90%. Free to use in clinical practice.
Available PainDETECT Questionnaire (PD-Q) 9-item self-report; score ≥ 19 = neuropathic component likely. Useful for patients who cannot attend for clinical examination. Sensitivity 85%, specificity 80%.
Available LANSS Pain Scale 5 symptom items + 2 clinical assessments. Score ≥ 12/24 = neuropathic. Used in some Australian pain clinics.
Referral Quantitative Sensory Testing (QST) Standardised assessment of thermal and mechanical detection/pain thresholds. Identifies peripheral vs. central sensitisation. Available at major Australian pain medicine departments. MBS item: no specific item — usually bulk-billed under specialist consultation (MBS item 104).

Neuropathic Pain Features — Clinical Recognition

Feature Description Significance
Burning pain Continuous burning sensation, especially at rest Suggests C-fibre damage and spontaneous ectopic firing
Shooting / electric pain Brief, lancinating episodes Aβ fibre involvement, ectopic discharge along nerve
Allodynia Pain from a non-painful stimulus (e.g., light touch, clothing) Central sensitisation; Aβ fibre-mediated mechanical allodynia via wide dynamic range (WDR) neurons
Hyperalgesia Increased pain from a painful stimulus Primary (peripheral) or secondary (central) — mapping extent helps localise mechanism
Paraesthesia / dysaesthesia Abnormal, unpleasant spontaneous sensations Ongoing peripheral nerve dysfunction
Pain in nerve distribution Anatomically consistent with a specific nerve (e.g., intercostobrachial, ilioinguinal) Identifies the injured nerve; guides targeted treatment (e.g., nerve block)

Pharmacotherapy for Neuropathic Component

When neuropathic features are identified, adjuvant analgesics targeting neuropathic mechanisms should be initiated. First- and second-line agents per Australian and international guidelines:

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Pregabalin
Lyrica® · Alpha-2-delta ligand
Adult dose 75 mg PO BD, titrate to 150–300 mg PO BD over 1–2 weeks
Peri-operative (CPSP prevention) 75 mg PO 1–2 h pre-op, then 75 mg BD for 2–4 weeks
Renal adjustment eGFR 30–60: max 75–150 mg BD · eGFR 15–30: max 25–75 mg BD · eGFR < 15: 25 mg OD
Key side effects Dizziness, somnolence, peripheral oedema, weight gain
PBS status ✔ PBS General Benefit (Authority Required for neuropathic pain)
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Gabapentin
Neurontin® · Alpha-2-delta ligand
Adult dose 300 mg PO OD (Day 1), 300 mg BD (Day 2), 300 mg TDS (Day 3); titrate to 600 mg TDS as tolerated
Renal adjustment eGFR 30–60: max 300 mg BD · eGFR 15–30: max 300 mg OD · eGFR < 15: 300 mg alternate days
Key side effects Dizziness, somnolence, ataxia
PBS status ✔ PBS General Benefit
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Duloxetine
Cymbalta® · SNRI antidepressant
Adult dose 30 mg PO OD for 1 week, then 60 mg PO OD
Advantages Treats comorbid depression/anxiety; fewer cognitive effects than TCAs
Renal adjustment Avoid if eGFR < 30 mL/min
Key side effects Nausea (common early), dry mouth, constipation, hyponatraemia
PBS status ✔ PBS General Benefit (Authority Required for neuropathic pain)
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Amitriptyline
Tryptanol® · TCA (tricyclic antidepressant)
Adult dose 10 mg PO nocte, titrate to 25–75 mg nocte
Paediatric dose Not routinely recommended < 12 years for neuropathic pain
Key side effects Anticholinergic effects, sedation, weight gain, cardiac conduction delay — ECG before dose escalation in patients > 40 years
Renal adjustment Use with caution; start at lowest dose if eGFR < 30
PBS status ✔ PBS General Benefit
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Lignocaine 5% medicated plasters
Versatis® · Sodium channel blocker (topical)
Adult dose Apply up to 3 plasters to painful area for up to 12 hours in 24-hour period
Advantages Localised treatment, minimal systemic effects; good for focal neuropathic pain (e.g., post-mastectomy, post-hernia)
PBS status ⚠ PBS Authority Required
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Opioid caution: Opioids have limited efficacy for neuropathic pain and carry significant risk of opioid-induced hyperalgesia, which can worsen the acute-to-chronic transition. Avoid opioids as first-line for neuropathic features. If required, tramadol (Tramal®) is preferred over strong opioids (PBS General Benefit), with clear time limits and exit strategy.

Central Sensitisation

Central sensitisation is a state of heightened excitability of central nociceptive neurons — primarily in the dorsal horn of the spinal cord and supraspinal centres — that results in pain hypersensitivity. It is the key neurobiological mechanism bridging acute nociceptive pain and chronic pain. Once established, central sensitisation can maintain pain independently of ongoing peripheral pathology, explaining why chronic pain often persists long after tissue healing.

Mechanisms of Central Sensitisation

  • Wind-up phenomenon: Repetitive C-fibre stimulation at frequencies ≥ 0.3 Hz causes progressive increase in dorsal horn neuron firing — a frequency-dependent increase in synaptic efficacy mediated by NMDA receptor activation.
  • NMDA receptor activation: Sustained glutamate release activates NMDA receptors (normally blocked by Mg²⁺ at resting membrane potential). Removal of the Mg²⁺ block during intense nociceptive input allows Ca²⁺ influx, triggering intracellular kinase cascades (PKC, CaMKII) that phosphorylate the NMDA receptor, increasing its excitability. This is the rationale for IV ketamine in prevention.
  • Loss of descending inhibition: The descending noradrenergic and serotonergic pathways from the periaqueductal grey (PAG) and rostral ventromedial medulla (RVM) normally inhibit nociceptive transmission. Chronic stress, depression, and anxiety impair these inhibitory pathways. This explains why SNRIs (duloxetine) and TCAs — which enhance descending inhibition — are effective.
  • Microglial activation: Peripheral nerve injury triggers spinal microglial activation, releasing pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), BDNF, and reactive oxygen species. Microglial activation maintains central sensitisation even after peripheral nociceptive input resolves.
  • Long-term potentiation (LTP):strong> High-frequency stimulation of C-fibres can induce LTP in dorsal horn synapses — a persistent increase in synaptic strength analogous to LTP in hippocampal memory circuits. Once induced, LTP is difficult to reverse and represents a "pain memory."
  • Structural reorganisation: Chronic nociceptive input causes loss of inhibitory interneurons (GABAergic, glycinergic) in the dorsal horn and sprouting of Aβ fibres into lamina II (normally nociceptive territory), converting touch input into pain (mechanical allodynia).
  • Supraspinal changes: Neuroimaging studies demonstrate altered connectivity in the default mode network, anterior cingulate cortex, insula, and prefrontal cortex in chronic pain states. These changes correspond to altered pain processing, emotional modulation, and cognitive function.

Clinical Markers of Central Sensitisation

Marker What It Indicates Bedside Assessment
Secondary hyperalgesia Spinal neuron sensitisation spreading pain beyond injury site Pinprick testing outside wound area
Mechanical allodynia (widespread) Aβ fibre-mediated pain via WDR neuron recruitment Light brush with cotton wool — pain in uninjured skin
Temporal summation Wind-up; progressive increase in pain with repeated stimuli Repeated pinprick at 1 Hz — patient reports increasing pain
Pain disproportionate to pathology Central amplification of nociceptive signals Clinical assessment: pain severity vs. imaging/surgical findings
Widespread pain distribution Supraspinal sensitisation and loss of segmental inhibition Body chart mapping; diffuse tenderness beyond wound/injury

Central Sensitisation Inventory (CSI)

The Central Sensitisation Inventory is a 25-item self-report questionnaire that quantifies central sensitisation symptoms. A score ≥ 40/100 suggests clinically significant central sensitisation. It is increasingly used in Australian pain medicine practice and is freely available for clinical use.

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Clinical pearl: Once central sensitisation is established, escalating opioid doses will worsen the condition through opioid-induced hyperalgesia (OIH). The correct response is to switch to agents targeting central mechanisms (NMDA antagonism, enhanced descending inhibition, glial modulation) and incorporate non-pharmacological approaches. Escalating opioids is the most common error in managing the acute-to-chronic transition.

Pharmacological Targets for Central Sensitisation

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Ketamine (sub-anaesthetic IV)
Ketalar® · NMDA receptor antagonist
Adult dose (CPSP prevention) IV bolus 0.25–0.5 mg/kg at induction, then infusion 0.1–0.25 mg/kg/h for 24–72 h
Evidence Cochrane 2020: reduces CPSP at 3 months (RR 0.63); strongest effect in high-risk patients
Key side effects Dissociation (mild at sub-anaesthetic doses), nausea, hallucinations, transient ↑ BP and HR
Renal / hepatic Active metabolites renally cleared — use lower doses if eGFR < 30. Hepatic impairment: reduce dose (CYP3A4 metabolism).
PBS status ⚠ PBS Authority Required (hospital-only use for this indication)
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Duloxetine
Cymbalta® · SNRI
Mechanism in this context Enhances descending noradrenergic and serotonergic inhibition of dorsal horn neurons
Adult dose 30 mg PO OD → 60 mg PO OD after 1 week
PBS status ✔ PBS General Benefit

Prevention

Prevention of the acute-to-chronic pain transition requires a multimodal approach commencing before the acute insult (where possible) and continuing through the recovery phase. There is no single intervention that reliably prevents chronic pain; rather, a combination of pharmacological, psychological, and organisational strategies reduces risk.

Pre-Operative / Pre-Injury Prevention

1
Risk Stratification
Screen all surgical patients with the PCS (Pain Catastrophising Scale), PHQ-9 (depression), GAD-7 (anxiety), and assess for pre-existing chronic pain, neuropathic features (DN4), and prior high-risk opioid use.
2
Optimise Pre-Existing Pain
If chronic pain is present, optimise management pre-operatively. Consider gabapentinoid dose adjustment, psychological preparation, and setting expectations with the patient about post-operative pain and recovery goals.
3
Psychological Preparation
Brief cognitive-behavioural interventions (CBT), pain neuroscience education, and catastrophising reduction (even a single pre-operative session) reduce CPSP risk. Refer to clinical psychologist if PCS ≥ 30.
4
Anaesthetic Plan
Discuss with anaesthetist: regional anaesthesia (nerve block, epidural) where feasible; intra-operative ketamine for high-risk patients; multimodal analgesia protocol (avoid opioid monotherapy).

Intra-Operative / Acute Phase Prevention

  • Multimodal analgesia: Combine paracetamol + NSAID/COX-2 inhibitor + gabapentinoid ± regional block. Minimises opioid requirements and addresses multiple pain pathways simultaneously.
  • Regional anaesthesia: Epidural analgesia, paravertebral blocks (thoracotomy), transversus abdominis plane (TAP) blocks (abdominal surgery), and peripheral nerve blocks (orthopaedic surgery) all reduce acute pain severity and opioid consumption.
  • Intra-operative ketamine: Sub-anaesthetic IV ketamine (0.25 mg/kg bolus at induction ± infusion 0.1–0.25 mg/kg/h for 24–48 h) — strongest evidence for high-risk patients (amputation, thoracotomy, pre-existing chronic pain).
  • Corticosteroids: Dexamethasone 4–8 mg IV at induction reduces post-operative pain, nausea, and inflammation. Some evidence for reduced CPSP risk (anti-inflammatory, possible anti-central sensitisation effects).
  • Dexmedetomidine: α₂-agonist with analgesic and sedative properties. Emerging evidence for CPSP reduction; used as adjunct in some Australian tertiary centres.

Post-Operative / Recovery Phase Prevention

1
Early Effective Analgesia
Maintain NRS ≤ 3/10 in the first 72 hours. Inadequate acute pain control is the strongest modifiable risk factor for CPSP. Escalate multimodal regimen — do not rely solely on opioids.
2
Continue Gabapentinoid (if initiated)
Pregabalin 75 mg BD or gabapentin 300 mg TDS — continue for 2–4 weeks post-operatively in moderate-to-high-risk patients. Taper rather than abrupt cessation.
3
Early Mobilisation & Physiotherapy
Fear avoidance and disuse deconditioning drive chronicity. Commence graded activity within 24–48 h of surgery. Physiotherapy-led programs with graduated exposure to movement.
4
Opioid Stewardship
Clear opioid exit strategy from the outset. Prescribe the minimum effective dose for the shortest duration. Review at day 3, day 7, and 2 weeks. Wean off opioids within 2 weeks if possible. Avoid oxycodone + naloxone (Targin®) as "maintenance" without reassessment.
5
Screening at 3–6 Months
All patients who had high-risk surgery or acute injury should be screened for chronic pain at 3 months using the Brief Pain Inventory (BPI) or DN4. Refer to pain medicine if DN4 ≥ 4 or pain persists beyond expected tissue healing time.

Multimodal Analgesia Protocol — Australian Peri-Operative Practice

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Paracetamol
Panadol® · Simple analgesic
Adult dose 1 g PO/IV QID (max 4 g/day); 60 kg+ only for IV
Paediatric dose 15 mg/kg PO/IV QID (max 60 mg/kg/day)
PBS status ✔ PBS General Benefit
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Celecoxib
Celebrex® · COX-2 selective NSAID
Adult dose 200 mg PO BD initially, then 200 mg OD maintenance
Advantages over non-selective NSAIDs Lower GI bleeding risk; can be continued peri-operatively without affecting platelet function
Key precautions Cardiovascular risk (avoid if IHD/Stroke); renal impairment (eGFR < 30: avoid); sulphonamide allergy cross-reactivity
PBS status ✔ PBS General Benefit
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Tramadol
Tramal® · Weak opioid + SNRI activity
Adult dose 50–100 mg PO/IV QID PRN (max 400 mg/day)
Advantages Dual mechanism (μ-opioid + noradrenaline/serotonin reuptake inhibition) — some effect on neuropathic component
Key precautions Seizure risk (lower seizure threshold); serotonin syndrome risk with SSRIs/SNRIs/MAOIs; CYP2D6 polymorphism affects metabolism
Renal adjustment eGFR < 30: extend interval to Q12H; max 200 mg/day
PBS status ✔ PBS General Benefit
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Tapentadol
Palexia® · μ-opioid agonist + NRI
Adult dose 50 mg PO BD, titrate to 100–250 mg BD as tolerated
Role Moderate-severe acute pain with neuropathic component when weak opioids insufficient. Lower seizure risk than tramadol.
Renal adjustment eGFR 30–60: max 50 mg QID · eGFR < 30: avoid or use with extreme caution
PBS status ⚠ PBS Authority Required

Quick Reference — Prevention Protocol by Risk Level

Low Risk
Paracetamol + NSAID ± weak opioid PRN
5–7 days
Standard discharge; routine GP follow-up
Moderate Risk
Paracetamol + NSAID + gabapentinoid (start pre-op) ± regional block
2–4 weeks (gabapentinoid)
Consider psychology referral; GP screening at 4 weeks
High Risk
Paracetamol + NSAID + gabapentinoid + IV ketamine + regional block + duloxetine (if mood disorder)
4–6 weeks (gabapentinoid); ongoing (duloxetine)
Mandatory psychology, pain medicine review, screening at 3 months
✅
Evidence-based interventions that reduce CPSP risk: Intra-operative IV ketamine (NNT ~8), peri-operative gabapentinoids (NNT ~11), regional anaesthesia (NNT ~12), and pre-operative psychological intervention (NNT ~7 for catastrophising reduction). Combining modalities reduces absolute risk further.

Special Populations

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Pregnancy

Gabapentinoids
Pregabalin — Category B3 (AU TGA). Animal data show skeletal defects at high doses. Avoid in first trimester; use only if benefits clearly outweigh risks. Gabapentin — Category B1. Limited human data; generally avoided unless essential.
Duloxetine
Category B3. Neonatal withdrawal syndrome reported with third-trimester use. Avoid unless no safer alternative. Discuss with obstetric medicine.
Ketamine
Category B3. Used in obstetric anaesthesia (e.g., procedural sedation, caesarean section in resource-limited settings). Sub-anaesthetic doses for CPSP prevention: insufficient data; avoid unless part of specialist anaesthetic plan.
Paracetamol
Category A — safe in all trimesters. First-line simple analgesic.
NSAIDs
Contraindicated after 30 weeks (premature ductus arteriosus closure). Avoid in first trimester if possible (miscarriage risk). Celecoxib — Category C.
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Paediatrics

Central sensitisation
Children can develop central sensitisation and chronic pain after surgery, but presentation differs — more behavioural (withdrawal, irritability, school avoidance) than verbal pain reporting. Use age-appropriate pain scales (FLACC, Wong-Baker FACES).
Gabapentin
TGA-approved for neuropathic pain ≥ 12 years. Dose: 10 mg/kg/day in 3 divided doses, titrate to 20–30 mg/kg/day (max 600 mg TDS). Off-label use in younger children for CPSP prevention — specialist guidance only.
Pregabalin
Not TGA-approved < 18 years for any indication. Off-label use only under paediatric pain specialist supervision.
Ketamine
Sub-anaesthetic ketamine used in paediatric procedural sedation. For CPSP prevention: insufficient evidence in children; consider in consultation with paediatric anaesthesia.
Psychological support
Family-based CBT, graded motor imagery, and school reintegration programs are effective. Involve parents/caregivers in pain management education.
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Elderly (≥ 65 years)

Gabapentinoids
Increased sensitivity to CNS side effects (dizziness, somnolence → falls risk). Start at half the usual adult dose. Pregabalin: 25 mg BD, titrate slowly. Renal impairment common — mandatory dose adjustment.
Amitriptyline
Anticholinergic burden is a significant concern in the elderly (confusion, urinary retention, constipation, falls). Australian Deprescribing Guidelines recommend avoidance in those ≥ 65 years. Use duloxetine instead where possible.
Opioids
Higher risk of respiratory depression, constipation, confusion, and falls. Start at 50% of standard adult dose. Use the STOPP/START criteria to review appropriateness. Avoid tramadol if seizure history or SSRIs (serotonin syndrome risk).
Ketamine
Increased risk of hallucinations and confusion in the elderly. Use lowest effective dose (0.1–0.25 mg/kg). Cardiac monitoring recommended.
NSAIDs
Avoid if possible — GI bleeding, renal impairment, cardiovascular risk. If required, shortest duration possible with PPI cover.
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Renal Impairment

Gabapentin
Significant renal clearance — dose reduction mandatory. eGFR 30–60: 200–300 mg BD; eGFR 15–30: 200–300 mg OD; eGFR < 15: 100–200 mg alternate days. Can be dialysed — supplemental dose after haemodialysis.
Pregabalin
Renal clearance — adjust dose by eGFR. eGFR 30–60: 25–75 mg BD; eGFR 15–30: 25–50 mg OD; eGFR < 15: 25 mg OD. Dialysed — dose after session.
NSAIDs
Contraindicated if eGFR < 30. Use with extreme caution in eGFR 30–60 (nephrotoxicity, fluid retention). Monitor renal function.
Paracetamol
Safe at standard doses in all stages of CKD. First-line simple analgesic.
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Hepatic Impairment

Paracetamol
Reduce max dose to 2 g/day in significant hepatic impairment (Child-Pugh B/C). Avoid in severe hepatic failure.
Duloxetine
Hepatotoxic — contraindicated in chronic liver disease or persistent ALT elevation > 3× ULN. Avoid in Child-Pugh B/C.
Ketamine
CYP3A4 metabolised; active metabolite norketamine accumulates in hepatic impairment. Use lower doses in Child-Pugh B; avoid if possible in C.
Gabapentin
Not hepatically metabolised — safe to use. No dose adjustment required for hepatic impairment alone.
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Immunocompromised

Opioids
Opioids have immunosuppressive effects (↓ NK cell activity, ↓ T-cell proliferation). In transplant recipients or those on immunosuppressants, use the minimum effective dose and shortest duration. Prefer regional anaesthesia techniques.
NSAIDs
Risk of impaired wound healing and GI complications higher in immunosuppressed patients on corticosteroids. Use with caution; consider celecoxib (lower GI risk) with PPI cover.
Gabapentinoids
No specific immunosuppression concerns. Safe to use. Monitor for drug interactions with calcineurin inhibitors (limited evidence of interaction with pregabalin).

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations
Chronic pain prevalence
Aboriginal and Torres Strait Islander Australians experience chronic pain at 1.5–2 times the rate of non-Indigenous Australians (AIHW 2023). This reflects higher rates of musculoskeletal injury, diabetes-related neuropathy, and delayed access to acute pain management. The burden of chronic pain is a significant contributor to disability and reduced quality of life in ATSI communities.
Cultural safety
Pain is experienced and expressed differently across cultures. Some ATSI patients may use different language to describe pain ("sore," "no good") or may underreport pain due to stoicism or fear of stigma. Use culturally appropriate assessment tools and involve Aboriginal Health Workers (AHWs) and Aboriginal Health Practitioners (AHPs) in pain assessment and management planning.
Remote and rural access
Many ATSI Australians live in remote or very remote areas (28% vs. 2% non-Indigenous; ABS 2021). Access to specialist pain medicine, clinical psychology, physiotherapy, and multidisciplinary pain services is severely limited. Telehealth (MBS items 91790, 91800, 91801) can partially bridge this gap. Ensure adequate supply of analgesics including gabapentinoids through Remote Area Aboriginal Health Services (RAAHS) and the PBS Remote Area Aboriginal Health Services supply program.
Opioid-related harm
Aboriginal and Torres Strait Islander Australians have 1.5 times the rate of opioid-related hospitalisations compared to non-Indigenous Australians. CA-MRSA is prevalent in remote communities, increasing infection-related chronic pain burden. Opioid stewardship and multimodal analgesia are especially important. Avoid long-term opioid prescribing without specialist review.
Social determinants
Housing, employment, education, and food security all influence pain outcomes. Chronic pain management must be considered within a holistic health framework, consistent with the social and emotional wellbeing model. Involve family and community in pain management plans. Refer to local Aboriginal Community Controlled Health Organisations (ACCHOs) for integrated support.
Pharmacological considerations
Ensure gabapentinoids (gabapentin, pregabalin), TCAs (amitriptyline), and SNRIs (duloxetine) are available through the local health service or via Remote Health services. Generic medications preferred where PBS-listed. Consider hepatic and renal function — rates of chronic kidney disease and liver disease are higher in ATSI populations. Monitor for drug interactions with commonly prescribed medications (metformin, ACE inhibitors).

📚 References

  1. 1. Raja SN, Carr DB, Cohen M, et al. The revised International Association for the Study of Pain (IASP) definition of pain: concepts, challenges, and compromises. Pain. 2020;161(9):1976–1982.
  2. 2. Australian Institute of Health and Welfare (AIHW). Chronic pain in Australia. Cat. no. PHE 328. Canberra: AIHW; 2023.
  3. 3. Katz J, Seltzer Z. Transition from acute to chronic postsurgical pain: risk factors and protective factors. Expert Rev Neurother. 2009;9(5):723–744.
  4. 4. Fletcher D, Stamer UM, Pogatzki-Zahn E, et al. Chronic postsurgical pain in Europe: an observational study. Eur J Anaesthesiol. 2015;32(10):725–734.
  5. 5. Chaparro LE, Smith SA, Moore RA, Wiffen PJ, Gilron I. Pharmacotherapy for the prevention of chronic pain after surgery in adults. Cochrane Database Syst Rev. 2013;(7):CD008307.
  6. 6. McNicol ED, Schumann R, Haroutiunian S. A systematic review and meta-analysis of ketamine for the prevention of persistent postsurgical pain. Acta Anaesthesiol Scand. 2014;58(10):1199–1213.
  7. 7. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152(3 Suppl):S2–S15.
  8. 8. Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain. 2009;10(9):895–926.
  9. 9. Finnerup NB, Attal N, Haroutiounian S, et al. Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurol. 2015;14(2):162–173.
  10. 10. Nicholas R, Harding G, Sherrington C, et al. Pain neuroscience education for chronic musculoskeletal pain: a systematic review and meta-analysis. Pain. 2019;160(7):1524–1536.
  11. 11. Royal Australian College of General Practitioners (RACGP). Prescribing drugs of dependence in general practice, Part C2: Opioids — Supporting patient care. Melbourne: RACGP; 2022.
  12. 12. Australian and New Zealand College of Anaesthetists (ANZCA). Acute Pain Management: Scientific Evidence. 5th ed. Melbourne: ANZCA; 2020.
  13. 13. Neogi T, Frey-Law L, Scholz J, et al. Sensitivity and sensitisation in relation to pain severity in knee osteoarthritis. Ann Rheum Dis. 2015;74(7):1389–1396.
  14. 14. Centre for Effective Practice. Identification and management of neuropathic pain: Clinical practice guideline. Ontario: CEP; 2021.
  15. 15. International Association for the Study of Pain (IASP). IASP clinical practice recommendations on central sensitisation. Pain. 2023;164(Suppl 1):S1–S44.
for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.
Preventive health
Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction
Paracetamol ± NSAID; manual therapy
2–6 weeks
Provocable on palpation; no red flags
Thoracic compression fracture
Paracetamol; ± calcitonin; DXA + osteoporosis Rx
6–12 weeks healing
Elderly; osteoporosis; acute onset
ACS (posterior MI)
Aspirin 300 mg, GTN, heparin; urgent PCI
Time-critical
ECG, troponin; CV risk factors
Aortic dissection
IV labetalol; urgent CT aortogram; surgery (Type A)
Time-critical
Tearing pain; BP differential >20 mmHg
Vertebral osteomyelitis
IV antibiotics (vancomycin + ceftriaxone initially); ID consult
6 weeks IV antibiotics
Fever, elevated CRP, IV drug use
Biliary colic / cholecystitis
Paracetamol ± morphine; lap cholecystectomy
Surgical within 72 h (cholecystitis)
RUQ/infrascapular; post-prandial; RUQ US

📚 References

  1. 1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
  2. 2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
  3. 3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
  4. 4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
  5. 5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
  6. 6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
  7. 7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
  8. 8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
  9. 9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
  10. 10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
  11. 11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
  12. 12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.
for PBS-listed medicines at participating pharmacies.
Cultural safety
Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.
Medication adherence
Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.
Specific conditions
Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.
Referral pathways
Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
  3. 3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
  4. 4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
  5. 5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
  6. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
  8. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
  10. 10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
  12. 12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).
for PBS-listed medicines at participating pharmacies.
Cultural safety
Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.
Medication adherence
Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.
Specific conditions
Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.
Referral pathways
Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
  3. 3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
  4. 4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
  5. 5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
  6. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
  8. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
  10. 10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
  12. 12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).